MET EOYS1 Flashcards
What is A
Middle colic artery
Jejunal arteries
Ileal colic artery
Right colic artery
What is A
Middle colic artery
Jejunal arteries
Ileal colic artery
Right colic artery
Label A & B [2]
A Jejunal arteries
B Ileal arteries
Label A-E
A: Left colic artery
B: IMA
C: Ileal arteries
D: Ileocolic artery
E: Right colic artery
What is A?
Left colic artery
SMA
Middle colic artery
Ileocolic artery
Right colic artery
Middle colic artery
Which two points does the inguinal ligament run between? [2]
ASIS to pubic tubercle
Which two molecules can activate the adenylyl cyclase pathway, which causes glycogenlysis, GNG? [2]
Glucagon
Adrenaline
As the food bolus is pushed into the pharynx the epiglottis of the larynx is pulled inferiorly to prevent food being aspirated.
Which nerve is responsible for closure of the larynx?
Superior laryngeal nerve
Recurrent laryngeal nerve
Glossopharnygeal nerve
Vagus nerve
As the food bolus is pushed into the pharynx the epiglottis of the larynx is pulled inferiorly to prevent food being aspirated.
Which nerve is responsible for closure of the larynx?
Superior laryngeal nerve
Recurrent laryngeal nerve
Glossopharnygeal nerve
Vagus nerve
As the recurrent laryngeal nerve innervates all muscles of the larynx (except cricothyroid) it is responsible for the closure during swallowing.
describe the branches of the SMA (6)
- inferior pancreaticoduedenal artery
- jejnunal and ileal branches
3 middle colic artery
- right colic artery
- ileocolic artery -> appendicular artery
MRI !
Contrast-enhanced CT is performed with selected images shown. What is the most likely diagnosis?
Amyand hernia
De Garengeot hernia
femoral hernia
direct inguinal hernia
indirect inguinal hernia
obturator hernia
This 50-year-old man presents with abdominal pain. Abdominal x-ray shows small bowel dilatation. Contrast-enhanced CT is performed with selected images shown. What is the most likely diagnosis?
Amyand hernia
De Garengeot hernia
femoral hernia
direct inguinal hernia
indirect inguinal hernia
obturator hernia
Name the gene that causes polycystic kidney disease [1]
Describe the inheritance pattern [1]
PKD1 or PKD2
Autosomal dominant
Name two Calcineurin inhbitors [2]
Cyclosporin and tacrolimus
Prednisolone targets which cytokine gene activation? [1]
IL-2
Learn x
Which of the following targets IL-2 gene activation / suppresses IL-2 activation
Azathioprine
Prednisolone
Cyclosporin
Tcrolimus
Mycophenolic acid
Which of the following targets IL-2 gene activation / suppresses IL-2 activation
Azathioprine
Prednisolone
Cyclosporin
Tcrolimus
Mycophenolic acid
Immunosuppressant drugs
Which of the following are calcineurin inhibitors? [2]
Azathioprine
Prednisolone
Cyclosporin
Tacrolimus
Mycophenolic acid
Which of the following are calcineurin inhibitors? [2]
Azathioprine
Prednisolone
Cyclosporin
Tacrolimus
Mycophenolic acid
Describe the action of calcineurin [1]
Calcineurin is an enzyme that activates T-cells of the immune system.
How long should ischaemia be limited to prevent acute transplant rejection:
-Cold ischaemia? [1]
- Warm ischaemia? [1]
Cold ischaemia time: 12 hrs
Warm ishaemia time: 1 hour
Which gene causes this disease? [1]
Describe the structure that this gene predominately codes for [1]
Polycystin gene - codes for primary cilia
Conn’s syndrome causes which of the following effects
- increase sodium reabsorption; increase potassium excretion
- decrease sodium reabsorption; increase potassium excretion
- decrease sodium reabsorption; decrease potassium excretion
- decrease sodium reabsorption; decrease potassium excretion
Conn’s syndrome causes which of the following effects
- increase sodium reabsorption; increase potassium excretion
Conns syndrome: XS aldosterone
What are the triad of signs of Conns syndrome? [3]
hypokalemia, hypernatremia and metabolic alkalosis
Conns syndrome patient presents with
Respiratory alkalosis
Respiratory acidosis
Metabolic alkalosis
Metabolic acidosis
Conns syndrome patient presents with
Respiratory alkalosis
Respiratory acidosis
Metabolic alkalosis
Metabolic acidosis
This symptoms is suggestive of
Conns syndrome
Cushings syndrome
Addisons disease
Sunburn
This symptoms is suggestive of
Conns syndrome
Cushings syndrome
Addisons disease
Sunburn
Hyperpigmentation is characteristic and occurs in almost all patients.
Elevated ACTH and melanocyte-stimulating hormone are causative factors. It is believed that ACTH binds to the melanocyte receptors, which are responsible for pigmentation
Describe the ascent of the kidneys during development:
Where do they start from? [1]
Where do they finish? [1]
(Include vert levels)
Describe the ascent of the kidneys during development:
Where do they start from? [1]
Sacral region S1
Where do they finish? [1]
Lumbar region T12
(Include vert levels)
Why wont babies survive bilateral kidney agenesis? [2]
If kidneys dont develop then effects creation of amniotic fluid (reduced: oligohydramnios)
This causes failure of lung development
Describe pathophysiology of autosomal dominant polycystic kidney disease
How do cysts grow? [4]
Mutation on polycystin gene: involved in production in primary cilia (ciliopathy)
Primary cilia involved in cell adhesion, calcium transport and cell cycle.
Cysts growth:
- Cysts originates as dilations of intact tubule
- Increased proliferation of cyst epithelium
- Cyst epithelium becomes secretory resulting in increased fluid secretion into lumen of cyst
- Cyst enlarges and loses contact with nephron
Which variables are used for MDRD equation to measure clearance? [4]
Need:
Cretinine
Age
Gender
Ethnicity
Name and explain which transport protein in the thick ascending loop of Henle assists NaKCl2 transporter
Renal Outer Medullary potassium channel or ROMK
- K is AT pumped into the tubular lumen / urine to generate positive voltage within the cell (because less K+ in)
- This creates an overall voltage gradient of +80mV; from +10mV in the tubular lumen to -70mV in the tubular cell
- This voltage difference drives Na into the tubular cell via NaKCl2 transporter
what other function do macula dense cells do ? / what do they produce?
The macula densa cells also tonically produce prostaglandin PGE2
which acts on juxtaglomerular cells to stimulate renin release
low sodium levels = More prostaglandin = more renin
what is the location, function and mechanism of action for the NKCC2 channels?
NKCC2 (Na-K-Cl cotransporter channel
- location: thick ascending limb of the loop of Henle
- function: to get Na / Cl out of the ascending limb and into extracellular fluid
-
mechanism of action:
i) luminal walls of the epithelial cells allows sodium, potassium & chloride ions to move passively together down their concentration gradient into the cells that make thick ascending limb
ii) then, sodium is actively transported out into extracellular space by Na/K ATP-ase
iii) Cl- moves passively with the sodium
iv) most of K+ ions diffuse back into the lumen via K ion channels
https://www.youtube.com/watch?v=sapTNUtrPdY
How would you calculate a MUST score? [3]
How do you work out an Action Plan for MUST? [1]
MUST:
1. BMI
2. Weight Loss
3. Acute disease effect
4. Add scores for 1-3
5. Action Plan
If MUAC is less than [], BMI is likely to be underweight (<20 kg/m2)
If MUAC IS over [], BMI is likely to be overweight ( >30 kg/m2)
.
If MUAC is under 23.5, BMI is likely to be under 20 (underweight)
If MUAC IS >32, BMI is likely to be >30 (overweight)
It is a widely held belief that low albumin arises because of inadequate protein intake.
Explain what causes Hypoalbuminaemia in hospital? [2]
Cause in hospital: is inflammation and sepsis:
- increased C-Reactive Protein
- White Cell Count
- pyrexia
- infection
In these patients capillary walls become more ‘porous’ and albumin drifts out –> low plasma albumin
Low albumin often occurs in sick, malnourished patients, but it is not caused by poor intake
Which Ptx are at risk of refeeding syndrome? [1]
Which Ptx are at high risk of refeeding syndrome? [4]
Which Ptx are at very high risk of refeeding syndrome? [4]
Risk
* Any ptx with very little food for more than 5 days
High risk
ONE OF:
Any one the following;
* BMI less than 16
* Unintentional weight loss >15% in last 3-6 months
* Little or no nutritional intake for more than 10 days
* Low levels of K, PO, Mg prior to feeding
Very high risk
TWO OF THE FOLLOWING:
* BMI less than 18.5
* Unintentional weight loss >10% in last 3-6 months
* Little or no nutrition for more than 5 days
* A history of alcohol abuse or drug use including chemotherapy, antacids or diuretics
What are two mechanisms that acute rejection occurs?
Acute rejection can be either via:
Acute Cellular Rejection (ACR)
- Cytotoxic T lymphocyte response
- Macrophage response
OR
Acute Antibody Mediated Response (AMR)
- B lymphocyte response making antibodies (agaisnt MHC Class 1 /2 antigens or ABO blood group antigens)
Antibody-mediated rejection (AMR):
What are the main antigens targets of antibodies? [3]
Where does this mainly occur? [1]
Antibody targets:
* MHC (Class I & II): HLA antigens:
* ABO antigens
* MHC class I-related chain A (MICA)
Target location: endothelium - targets arteries and capillaries (because these are the cells first meet after transplantation)
With regards to acute rejection of transplants, how would you detect antibody prescence?
Detect antibody presence with complement: C4d
- The antibody-antigen complex activates the compliment system
- This produces C4d molecules (which forms covalent bonds with endothelial cells)
- C4d molecules are stained easily
- This shows that acute rejection has occurred
Staining for C4d is a very good proxy for detecting antibodies
What is criteria for diagnosis of acute antibody rejection? [3]
Evidence of acute renal injury on histology (often microvascular inflammation)
Evidence of antibody activity C4d staining in peritubular capillaries
Circulating anti-donor specific antibodies
Explain how AMR causes damage in hyperacute rejection
change from anti-coagulant to pro-coagulant state:
- antibodies bind to surface of epithelial cells: become pro-coagulant and clots form
- causes downstream infarction
- causes haem.
Summary of hyperacute rejection:
Within 1 hr you get [] infiltrate of peritubular capillaries
Within 12-24 hrs you get what effects? [2]
Within 1 hr you get neutrophils infiltrate of peritubular capillaries
Within 12-24 hrs you get intravascular coagulation and cortical necrosis
How can we prevent hyperacute rejection? [3]
- Use somone who is ABO compatabile (O is universal donor)
-
screen for preformed antibodies:
* Direct cross match: mix donor cells and recipient serum. Look for complement activation (positive is bad)
* Beads with bound HLA: look to see if recipient serum binds to HLA beads
What are the most important HLAs? [3]
HLA A
HLA B
HLA DR
Each have two genes
Explain how can you prevent acute rejection of transplants? [2]
HLA matching (make sure that not positive for match)
Minimising ischaemia-reperfusion injury:
- Ischaemia causes upregulation of adhesion molecules, which increases adhesion of leukocytes when blood is reperfused.
- More leukocytes increases chance of rejection, SO try and limit ischaemia time.
- Cold ischaemia time: 12 hrs
- Warm ishaemia time: 1 hour
What are the two pathways of allorecognition?
Direct:
* Recipient T-cells recognise allogenic APC (donor APCs) and cause aggressive imune response to foreign HLA
Indirect:
* The allogenic APCs are replaced with auto-APCs
* Some of the peptides presented by new auto-APCS are derived from shed HLA molecules
* Causes a more gentle immune response
Explain how activation of a helper T cell / CD4 cell occurs [3]
- T helper cell receptor recognising antigen from HLA
- Co-stimulation from another molecule
Both these signals activate nucleus to make IL-2.
IL-2 binds to IL-2 receptor on different T helper cell. [3]
Causes signal at nucleus to make proliferation of T-helper cells
What are the sites of action used for immunosuppressive drugs? [3] and what drugs used?
Calcineurin inhibitors:
* Calcineurin is an enzyme that activates T-cells of the immune system.
* E.g. Cyclosporin and tacrolimus (learn !)
Anti-proliferative drugs:
* (target nucleus at end stage of T cell activation)
* e.g. Azathioprine and Mycophenolic acid
Prevent cytokine (IL-2) gene activation
* Use cortiosteroids
* e.g. Prednisolone
Standard treatment: Calcineurin inhib, steroid and anti-proliferative drugs
Label A & B of developing kidneys
A: mesonephric bud
B: uteric bud
What type of renal pathology is depicted here?
IgA neuropathy
Membrane change disease
Glomerulonephritis
Acute rejection from kidney transplant
What type of renal pathology is depicted here?
IgA neuropathy
Membrane change disease
Glomerulonephritis
Acute rejection from kidney transplant
Focal glomerulitis in active antibody mediated rejection-Banff score g3. Dilated glomerular capillaries are filled with swollen endothelial cells and inflammatory cells (PAS, 200×).
GPR54 is involved in the stimulation of which pituitary hormone? [1]
GPR101 is involved in the stimulation of which pituitary hormone? [1]
GPR54: GnRH
GPR101: Growth Hormone
A woman is admitted with left-sided weakness and collapse. She is brought in with her husband, who explains that she has no drug allergies and a past medical history of diabetes, hyperthyroidism and autosomal dominant polycystic kidney disease.
A CT scan of the head shows a large, right-sided intracerebral bleed.
What is the most likely cause of the bleed?
Hypertension
Poorly controlled diabetes
Ruptured berry aneurysm
Atherosclerotic disease
Paradoxical embolism
Ruptured berry aneurysm
Adult polycystic kidney disease increases the risk of brain haemorrhage due to ruptured berry aneurysms
